our analysis continues to focus on specificity and selection of alpha beta T cell receptors (TCR alpha beta). We have be ' en examining mechanisms of T cell tolerance, and showed that in the absence of the thymus, the induction of T cell tolerance by clonal deletion is impaired. We have also found that staphylococcal enterotoxin B (SEB) can induce tolerance in mature peripheral T cells by clonal anergy such that murine V beta 8+ cells, that normally respond to SEB, persist in lymphoid organs after SEB priming but cannot proliferate in response to subsequent SEB challenge. If the molecular basis of this peripheral tolerance can be understood, it might be possible to modulate immune function in vivo in a TCR alpha beta specific fashion. Our structural analysis of TCR alpha beta function has continued. We have defined a single point mutation in the putative complementarity determining region I (CDR1) of the TCR beta chain that has a profound effect on antigen recognition. We are currently conducting modelling studies to determine the structural consequences of this point mutation.